The purpose of this project is to further define the biochemical basis of amoeboid movement, ingestion, and microbial killing by phagocytic cells. Based on the assumption that contractile proteins and microtubules are the driving force behind amoeboid movement, the plan is to isolate contracttle proteins from phagocytic cells. Since H2O2 attenuates ingestion by phagocytes, studies will be performed to investigate the effects of H2O2 and other oxygen by-products on consistency changes of solution brought about by the interaction of the contractile proteins. Myosin will be isolated from phagocytic cells and rates of actin activation of myosin Mg ions ATPase activity will be correlated with rates of ingestion. The effects of altering cellular glutathion levels on phagocyte function by depriving rates of selenium and microtubule assembly will be assessed. The effects of alpha tocopherol on protecting cellular microtubule integrity in human polymorphonuclear leukocytes deficient in glutathione will be studied. The effect of oligopeptides which are chemotactic for polymorphonuclear leukocytes on potentially inducing microtubule assembly will be monitored. Since oxidants attenuate polymorphonuclear leukocyte chemotaxis and phagocytosis, the effects of an O2-H2O2 scavenger, 2,3-dihydroxybenzoic acid on protecting the polymorphonuclear leukocyte from oxidant damage will be examined.